ArticleNature communications2021
Introns control stochastic allele expression bias.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Maternal histone methyltransferases antagonistically regulate autosomal random monoallelic expression (aRMAE) in C. elegans.Nature communications · 2025Article
- Pervasive Conservation of Intron Number and Other Genetic Elements Revealed by a Chromosome-level Genome Assembly of the Hyper-polymorphic Nematode Caenorhabditis brenneri.Genome biology and evolution · 2025Article
- Pervasive conservation of intron number and other genetic elements revealed by a chromosome-level genomic assembly of the hyper-polymorphic nematodebioRxiv : the preprint server for biology · 2024Article
- Transgressive and parental dominant gene expression and cytosine methylation during seed development in Brassica napus hybrids.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2023Article
- Random allelic expression in the adult human body.Cell reports · 2023Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Monoallelic expression (MAE) or extreme allele bias can account for incomplete penetrance, missing heritability and non-Mendelian diseases. In cancer, MAE is associated with shorter patient survival times and higher tumor grade. Prior studies showed that stochastic MAE is caused by stochastic epigenetic silencing, in a gene and tissue-specific manner. Here, we used C. elegans to study stochastic MAE in vivo. We found allele bias/MAE to be widespread within C. elegans tissues, presenting as a continuum from fully biallelic to MAE. We discovered that the presence of introns within alleles robustly decreases MAE. We determined that introns control MAE at distinct loci, in distinct cell types, with distinct promoters, and within distinct coding sequences, using a 5'-intron position-dependent mechanism. Bioinformatic analysis showed human intronless genes are significantly enriched for MAE. Our experimental evidence demonstrates a role for introns in regulating MAE, possibly explaining why some mutations within introns result in disease.
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